Exercise-induced increase of cardiac biomarkers in competitive-amateur soccer players: exploring troponin and NT-proBNP responses

Introduction

Background

Cardiac troponin (cTn) (I and T) is the gold standard marker for diagnosing acute coronary syndrome. The Fourth Universal Definition of Myocardial Infarction stated that a single cTn reading above the 99th percentile upper reference limit (URL) can be defined as myocardial injury, even in the absence of acute myocardial infarction (MI) (1). Therefore, cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are highly sensitive and specific markers not only of MI but of myocardial damage in general, with elevated levels associated with various cardiac events (e.g., myocarditis, heart failure, pericarditis, arrhythmias). Therefore, assessing and interpreting elevated troponin levels in the clinical context has become increasingly complex (2). Furthermore, several studies have observed that physiological conditions such as exercise can also lead to fluctuations in biomarkers.

In 2020, the guideline on sports cardiology and exercise from the European Society of Cardiology (ESC) established that transient elevations of high levels of cTn, above the 99th percentile URL, frequently occur and are also present in both athletes and healthy individuals under physical exercise stimuli (3). This phenomenon has been extensively documented across various sports disciplines and exercise intensities, suggesting that post-exercise troponin elevations may not necessarily indicate myocardial injury but rather reflect a physiological response to increased cardiac workload (4,5).

Although high levels of troponin are well known in high-intensity sports or among professional athletes, data on cardiac biomarkers in competitive amateur athletes remain poorly documented (6,7).

Rationale and knowledge gap

Recent research underscores the role of prolonged physical activity acts as a stressor on cardiac function, influencing the release of cardiac biomarkers, such as troponin and pro-brain natriuretic peptide (pro-BNP) (8). The magnitude of biomarkers fluctuations appears to be influenced by the intensity and duration of exercise, which are key factors in triggering this response, with studies showing that cTn levels (both cTnT and cTnI) rise significantly levels during and after 30–60 minutes of moderate to high/moderate intensity exercise, particularly in highly trained individuals and healthy subjects, such as competitive amateur athletes (9,10). For example, Perrone et al. showed a significant increase in high-sensitivity cardiac troponin I (hs-cTnI) and NT-proBNP in highly trained athletes after a 50 km ultramarathon race, and 30% of runners had the values of cardiac biomarkers above URL. These findings challenge traditional diagnostic paradigms, emphasizing the need for a nuanced interpretation of elevated troponin levels in physically active populations (6). One hypothesis for the post-exercise troponin increase is that it reflects reversible myocardial stress rather than acute myocardial injury.

In particular, the reversible myocardial stress may involve transient increases in cardiomyocyte membrane permeability, due to inflammatory responses, leading to the release of troponin into the circulation. Additionally, exercise-induced systemic inflammation and oxidative stress, involved in this process, further complicate the differentiation between physiological and pathological troponin (5,11). Despite these increases in cardiac biomarkers, multiple studies have reported no structural cardiac damage or abnormalities in electrocardiograms (ECGs) among athletes undergoing intense training regimens or endurance events (12-14).

In an effort to refine the clinical interpretation of cTn elevations in athletes, Li et al. proposed that analyzing the composition of troponin subtypes, particularly cTnT fragments, could provide additional insights (4). Their research suggests that differentiating cTn compositions, particularly cTnT fragments, may occur not only as a consequence of myocardial stress but also in response to additional, non-cardiac or non-ischemic factors. A specific ratio of long cTnT fragments to intact troponin complexes may therefore help distinguish acute ischemic injury from exercise-induced elevations, offering a potential strategy to reduce misdiagnoses in physically active individuals. This distinction suggests that in athletes, elevated cTn levels might not necessarily indicate pathological myocardial damage but rather a remodeling response to sustained cardiac strain. Thus, characterizing cTn fragments and their ratios could improve the interpretation of elevated cTn levels in athletes, reducing the risk of misdiagnosing myocardial injury when these elevations result from physiological adaptation rather than acute damage (8,15-17).

Objective

Understanding these fluctuations is particularly relevant given the increasing popularity of amateur sports and the growing number of individuals participating in high-intensity athletic events. This work would like to address the interpretation of exercise-induced elevations of cardiac biomarkers in competitive amateur athletes, a population that is still underrepresented in the sports cardiology literature compared with professional athletes. Our preliminary study aimed to evaluate the trend of cardiac biomarkers in male players from a competitive amateur soccer team during a match. By investigating biomarker dynamics in this population, we seek to contribute to the ongoing discussion regarding the physiological versus pathological significance of exercise-induced troponin elevations and their implications for sports cardiology. We present this article in accordance with the STROBE reporting checklist (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-78/rc).

Methods

Subjects and design of the study

The study was conducted in May 2025 with the support of a competitive soccer team competing in the First-Division recreational Italian championship, the highest level within the competitive non-professional soccer system. Before participation, all athletes provided informed consent through a written declaration. The Athlete Food Choice Questionnaire (AFCQ) was then administered to gather data on participants’ nutritional status, exercise training level, lifestyle factors (including supplement use, smoking habits, and health awareness) (18). The team was selected as a representative model of high-level competitive athletes, with rigorous training and standardized exercise protocols.

The study included 11 male participants of the soccer team, aged 18–30 years. All participants had undergone an annual mandatory pre-participation medical screening, which included spirometry, exercise ECG (cycle ergometer), urine analysis, medical history, physical examination, and assessment of blood pressure, body weight, and height, to ensure athlete safety. Four blood samples were taken: the first pre-match at rest (T1), as baseline, the second immediately after completing the 90-minute match (T2), the third 2 h after the second (T3), and the fourth 24-h post-match (T4). Between each blood collection, the athletes were hydrated. Blood samples were collected and immediately centrifuged on-site to ensure proper sample preparation. The samples were properly centrifuged at 2,000 g for 10 minutes. Following collection, the samples were transported under refrigerated conditions (2–8 ℃) to the Laboratory Medicine Department at University Hospital of the University of Rome “Tor Vergata” (Rome, Italy), for analysis.

The biochemical parameters analyzed at each time point included CK-MB, high-sensitivity troponin I (hs-TnI), NT-proBNP, insulin, blood cortisol, testosterone, and derivatives of reactive oxygen metabolites (D-ROMS).

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of the University Hospital Tor Vergata (ID No. 41.17), and all the participants signed an informed consent.

Biochemical analyses

The serum samples were analyzed using the Alinity c system (for CK-MB, NT-proBNP) and Alinity i system (for insulin, cortisol, hs-cTnI, testosterone) from Abbott Diagnostics (Chicago, IL, USA). Additionally, the testosterone/cortisol (T/C) ratio was calculated to assess the over-compensation rate. D-ROMS analysis, which measures oxidative stress, was performed using the Diacron kit (Diacron International, Grosseto, Italy) on the Cobas 8000 series analyzer (Roche Diagnostics International, Rotkreuz, Switzerland). Before the analysis session, quality controls were measured. The normal reference interval values were derived from the manufacturer’s technical documentation.

Statistical analyses

Descriptive analyses were conducted to summarize the data, utilizing central tendency and dispersion measures for continuous variables and frequency distributions for qualitative variables. For continuous variables that followed a normal distribution, measures such as the mean, standard deviation, and analysis of variance (ANOVA) with the Bonferroni post hoc test were utilized to assess differences between groups. In contrast, for continuous variables with a non-normal distribution, the median and percentiles were reported, and comparisons between paired groups were made using the Friedman test. If the Friedman test results in a P value less than this significance level, pairwise comparison of variables was performed (19). To assess whether the data followed a normal distribution, the Shapiro-Wilk test was performed, and a 95% confidence interval (CI) was applied. Statistical significance was considered at a P value of less than 0.05 for all tests.

Data were examined using MedCalc Ver.18.2.18 (MedCalc Software Ltd., Ostend, Belgium).

Results

Training information and clinical analysis

The results from the AFCQ questionnaire, with demographic data, presented in Table 1, indicate that the study population (n=11) maintains healthy habits, engages in high-moderate training, and has a balanced nutritional intake. Participants reported training four times a week, with each session being moderate in intensity (heart rate consistently within the target range) and lasting over 1 h (20). The median, 25th and 75th percentiles, and statistical significance of each biochemical parameter across the four blood collection time points are reported in Table 2. A significant difference was observed for CK-MB, insulin, and cortisol. The CK-MB median values (T1: 1.45 ng/mL, T2: 2.30 ng/mL, T3: 2.60 ng/mL, T4: 2.55 ng/mL) were significantly different between T1 (pre-match) and all other time points and significantly different between T2 and T3. The insulin median values (T1: 12.75 µU/mL, T2: 7.00 µU/mL, T3: 2.80 µU/mL, T4: 9.75 µU/mL) were significantly different between T3 (after 2 h from the match) and all other time points and between T1 and T2. The cortisol median values (T1: 8.3 µg/dL, T2: 12.9 µg/dL, T3: 6.2 µg/dL, T4: 6.9 µg/dL) were significantly different between T2 (post-match) and all other time points. Analogously, the T/C ratio median values (T1: 0.55, T2: 0.37, T3: 0.80, T4: 0.65) were significantly different between T2 (post-match) and all other times.

Troponin and NT-proBNP response

Figure 1 shows the trends of hs-cTnI and NT-proBNP. The median value of Troponin I at T2 (55.8 ng/L) was slightly higher compared to other time points (T1: 45.8 ng/L, T3: 43.8 ng/L, T4: 41.9 ng/L), with no substantial decrease and not significantly influenced by the match. However, the hs-cTnI values were persistently observed above the 99th percentile, at all time points. These baseline values may be attributed to the athletes’ regular training and ongoing physical exertion throughout the competitive season (see Table 1). Similarly, the NT-proBNP median value at T2 (110.0 pg/mL) was slightly higher than at T1 (88.7 pg/mL), T3 (107.0 pg/mL), and T4 (117.0 pg/mL), and its trend closely mirrored that of hs-cTnI, suggesting a comparable pattern of response to physical stress across the time points.

Figure 1 The trend for the 4 times of blood collection for the troponin I (A) and NT-proBNP (B), although not significant between each other. x-axis: times of blood collections; x sign: median value; dashed line: trend. **, P<0.01; ***, P<0.001. T1: pre-match. T2: post-match. T3: 2 hours post-match. T4: 24 hours post-match. CK, creatin kinase; D-ROMS, dynamic reactive oxygen metabolites; NT-proBNP, N-terminal pro-B-type natriuretic peptide.

Stress-related biomarkers

To further investigate the relationship between stress-related biomarkers, we examined whether the elevated levels of hs-cTnI and NT-proBNP were associated with changes in CK-MB, cortisol, and D-ROMS levels (21). In Figure 2A, we observed a significant increase in CK-MB levels from T1 to subsequent time points (T2, T3, and T4), indicating a response to physical exertion. Figure 2B shows a notable rise in cortisol levels at T2, further suggesting physiological stress following the match. On the other hand, D-ROMS levels, depicted in Figure 2C, though not statistically significant, were consistently above the normal range (250–300 U-CARR), indicating oxidative cellular stress. The D-ROMS values were as follows: T1 at 307 U-CARR, T2 at 332 U-CARR, T3 at 340 U-CARR, and T4 at 332 U-CARR.

Figure 2 The trend at the 4 times for stress-related analytes. (A) CK-MB levels. (B) Cortisol levels. (C) D-ROMS. x-axis: times of blood collections; x sign: median value; dashed line: trend. **, P<0.01; ***, P<0.001. T1: pre-match. T2: post-match. T3: 2 hours post-match. T4: 24 hours post-match. CK, creatin kinase; D-ROMS, dynamic reactive oxygen metabolites; hs-cTnI, high-sensitivity cardiac troponin I; NT-proBNP, N-terminal pro-B-type natriuretic peptide.

Overtraining ratio

Once we observed that our subjects were influenced by stress, we calculated the overtraining rate based on the testosterone/cortisol ratio (22). The soccer players showed an inverted pattern of distribution compared to cortisol levels: the T/C ratio was significantly lower immediately after the match (T2) and increased 2 h post-match (T3) (Table 2). The pre-match (T1) and 24-h post-match (T4) values were similar for most participants, although slightly increased afterward. Notably, the baseline median values (T1: 0.55) fell within the 0.51–0.65 range, indicating a moderate risk of overtraining (22,23).

Discussion

Key findings

Post-exercise increased troponin levels are well documented, with athletes typically exhibiting elevations that fall within the lower pathological range compared to those seen in cardiovascular diseases (24). The underlying mechanisms behind this release remain unclear; nevertheless, some works have focused on increased sarcolemma permeability and enhanced cardiomyocyte turnover (20,25). These chronic exercise-related myocardial stresses suggest that regular high-intensity training may influence myocardial stress markers in ways that differ from pathological conditions.

According to the American Heart Association, exercise-related risk is defined as a prolonged release of troponin above the 99th percentile, even in athletes. These persistently high levels may be the result of maladaptation after intensive and strenuous training, leading to an irreversible situation (26). Nevertheless, a reversible condition, characterized by high cTn values for a brief period (within 48 h), is more frequent in non-professional athletes (25,27). In this context, our findings indicated elevated troponin levels both at baseline and 24 h post-match, likely resulting from consistent and rigorous training of the soccer players. However, the findings from the AFCQ questionnaire suggested that the athletes have a well-established routine that supports both their physical and nutritional well-being, contributing to their overall fitness and readiness for competition.

The minimal fluctuations in hs-TnI and NT-proBNP trends may suggest that high-intensity exercise training has an influence on these parameters. However, there were no significant differences either before or after the match, supporting the hypothesis that prolonged exposure to vigorous activity results in biomarker increase without any clinically significant consequence.

Along with the troponin, the high NT-proBNP levels in this cohort may represent early signs of chronic exercise-induced stress or overtraining in some individuals. This contrasts with the generally stable NT-proBNP levels observed in acute settings among professional athletes, where the intensity and training conditions differed significantly (28-30).

Other parameters that could provide insights into cellular stress are CK-MB and cortisol levels. During the match, CK-MB levels increased due to cardiac stress and muscle exertion. More interestingly, these levels remained high even 24 h later. These results are consistent with previous studies (31,32). Similarly, cortisol levels increased during the match, which is a physiological response to physical effort (21,33). Additionally, D-ROMS levels, which indicate oxidative stress, also increased, further emphasizing the physiological impact of sustained high-intensity exercise. These findings suggest that the biomarker levels, particularly in CK-MB, cortisol, and D-ROMS, reflect the athletes’ physiological response to the stress induced by the continuous training under the competitive season without a proper post-exercise recovery.

Furthermore, considering these results, we also assessed the T/C ratio. Even in this case, our results showed that for most players, the baseline ratio fell within the 0.35–0.65 range, highlighting a high/moderate risk of overtraining rather than an appropriate training adaptation.

Strengths and limitations

The present work supports the concept that high-intensity exercise induces measurable systemic adaptations even in non-athletic populations. These findings reinforce the conceptualization of exercise as a robust physiological stressor and provide critical contextual reference for comparisons with intermittent, high-intensity sports, as already demonstrated in the literature (34,35). Moreover, these findings may offer a useful framework for comparison with intermittent, high-intensity sports, helping to contextualize how sustained training load and repeated metabolic stress could be associated with modest variations in cardiac biomarker levels.

Nevertheless, this study has several limitations that should be acknowledged. First, given its cross-sectional design and the focus on the physiological response to a single match, it is not possible to conclude the impact of chronic or season-long training on baseline biomarker levels. Although the relatively high baseline values observed may reflect chronic exercise-related myocardial stress in trained individuals, this interpretation remains speculative and is based on existing literature rather than directly supported by our data. Considering the persistent cTn high levels in healthy subjects, it would be interesting to increase the monitoring time of the athletes in further investigations. This could give a focused clarification on these biomarkers’ alterations. A longer observation window would provide deeper insights into the temporal evolution of these biomarkers and their potential implications.

Additionally, the relatively small sample size represents a limitation of this study. However, the number of participants was intrinsically constrained by the size of the soccer team itself (n=11). Moreover, the absence of a control group should be considered when interpreting these findings, as it may limit the strength of contextualization.

Comparison with similar research

Our results seem to underline that competitive amateur players exhibit high troponin values after prolonged exercise training, like professional athletes (6,36). Recent studies have shown that soccer players can have high troponin values in a training-dependent way without evidence of cardiac damage (37,38). This could help explain the pathophysiology of reversible vs. irreversible myocardial damage (39), also known as “troponin leak” (40).

Understanding this distinction is essential for clinicians to accurately interpret above 99^th percentile URL troponin levels in athletes, preventing unnecessary clinical concern and distinguishing between physiological alteration and potential maladaptive responses.

Explanations of findings

Therefore, the above 99^th percentile URL troponin levels in our cohort may be due to continuous training throughout the competitive season. In this framework, the hs-cTnI and NT-proBNP trends observed in our cohort are consistent with previously described non-pathological patterns. On the other hand, a methodological assessment should be conducted before making any further hypotheses. Differentiating between intact/fragmented and complex cTn could offer promising advancements in understanding and interpreting troponin levels. Some studies proposed the troponin differentiation as a valuable tool to improve the interpretation of increased troponin concentrations, particularly in athletes and patients with overlapping physiological and pathological cardiac stress markers (4,41-43), as well as assay variability (44,45).

Understanding the nuances of troponin fragmentation patterns and NT-proBNP dynamics provides a clearer perspective for assessing the differential etiology of excessive physical activity.

The T/C ratio finding is concerning, as chronic exposure to elevated cortisol levels and an imbalanced T/C ratio can contribute to prolonged recovery times, decreased performance, and an increased risk of injury. Continuous training, without supervision by a professional staff or a proper coach, could lead to excessive stress on these values, resulting in maladaptation.

Implications and actions needed

Additionally, implementing advanced imaging techniques, such as cardiac magnetic resonance imaging (MRI) or echocardiography, alongside biomarker assessments, could help clarify the clinical significance of these increases. This integrated approach may enable a more precise distinction between physiological adaptation and early signs of cardiac strain, ultimately contributing to improved training protocols and athlete health monitoring.

Conclusions

This study investigated biomarker variations in amateur soccer players before and after a match. Results showed minimal fluctuations for troponin I (hs-TnI) and NT-proBNP levels but shifted baseline levels. The results may indicate chronic exercise-related myocardial stress and cardiac fatigue in the athletes, although differentiating between intact, fragmented, and complex cTn could provide a more comprehensive understanding in the future.

Figure 3 Behavior of T/C ratio for each time observed. Each color identifies a single athlete. X-axis: times of blood collections. T1: pre-match. T2: post-match. T3: 2 hours post-match. T4: 24 hours post-match. T/C, testosterone/cortisol.

Acknowledgments

The authors would like to thank all the Clinical Biochemistry Laboratory staff of Tor Vergata Hospital for their support.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-78/rc

Data Sharing Statement: Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-78/dss

Peer Review File: Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-78/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-78/coif). M.P. serves as an unpaid editorial board member of Journal of Laboratory and Precision Medicine from January 2025 to December 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of the University Hospital Tor Vergata (ID No. 41.17), and all the participants signed an informed consent.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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